The H6PD Knockout KYSE-150 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population with disrupted H6PD. This pool of gene-edited cells derives from the KYSE-150 human esophageal squamous cell carcinoma line, providing a genetically heterogeneous model for studying H6PD loss-of-function. The polyclonal format avoids clonal selection bias and better represents population-level responses, making it suitable for investigating hexose-6-phosphate dehydrogenase (H6PD)-dependent processes such as endoplasmic reticulum (ER) redox homeostasis and glucocorticoid metabolism.
The KYSE-150 cell line originates from a well-differentiated human esophageal squamous cell carcinoma and is widely used in cancer research. These cells retain malignant features of esophageal epithelial carcinoma, including metabolic reprogramming and redox adaptation. In this context, H6PD knockout enables examination of how disrupted ER NADPH generation impacts tumor cell physiology. The adherent KYSE-150 line supports diverse functional and biochemical assays.
H6PD encodes an ER-lumen enzyme that oxidizes glucose-6-phosphate to produce NADPH, a cofactor essential for 11??-hydroxysteroid dehydrogenase type 1 (11??-HSD1) activity. 11??-HSD1 utilizes H6PD-generated NADPH to convert cortisone into cortisol, linking glucose metabolism to glucocorticoid activation. H6PD is regulated by glucose-6-phosphate availability and insulin signaling, and it interacts directly with the glucose-6-phosphate transporter and 11??-HSD1. Downstream, H6PD influences cortisol production, ER oxidoreductases, and redox-sensitive transcription factors. Thus, H6PD sits at the nexus of redox control and hormone metabolism.
In esophageal cancer cells, H6PD deficiency disrupts ER NADPH supply, impairing 11??-HSD1-mediated cortisol synthesis and potentially altering redox homeostasis. This can trigger ER stress and affect pathways controlling proliferation and survival. The KYSE-150 knockout model allows dissection of how cancer cells adapt to NADPH depletion and altered glucocorticoid signaling, revealing vulnerabilities that may be exploited therapeutically.
This polyclonal knockout product supports applications such as NADPH quantification, 11??-HSD1 activity assays, and LC-MS-based cortisol/cortisone profiling to evaluate glucocorticoid metabolism. Researchers can assess cell viability under oxidative stress, measure glucose-6-phosphate uptake, and perform transcriptomic analyses of redox and glucocorticoid-responsive genes. Western blotting for H6PD and 11??-HSD1 confirms target disruption. The model aids in studying cortisone reductase deficiency and related metabolic disorders. For additional details, contact Ascent Research.
